Afterload Reducers
Reduced systemic vascular resistance increases cardiac output and improves renal perfusion, allowing for diuresis.
Captopril
Captopril prevents the conversion of angiotensin I to angiotensin II. It is a potent vasodilator that lowers aldosterone secretion. It is an option in patients who are unable to tolerate NTG (eg, concurrent use of sildenafil). Hemodynamic (improved afterload and cardiac output) and subjective (decreased dyspnea) improvements occur in 10-15 minutes. Although captopril is not specifically formulated for sublingual (SL) use, the tablet can be wetted before it is placed under the patient's tongue to achieve the desired effect.
Enalapril (Vasotec)
Enalapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion. The use of IV captopril to treat decompensated heart failure and pulmonary edema not been studied as well as SL captopril has.
In 1993, Varriale evaluated patients with severe CHF and mitral regurgitation; he observed improved preload, afterload, cardiac output, and magnitude of regurgitation. In 1996, Annane evaluated patients with acute CPE and found improvements in preload and afterload. There was no demonstrated effect on cardiac output. Both studies showed an excellent safety profile.
Nitroprusside (Nitropress)
Nitroprusside is a potent, direct smooth muscle–relaxing agent that primarily reduces afterload but can mildly reduce preload. It improves cardiac output but can precipitously decrease blood pressure. Intra-arterial blood pressure monitoring is strongly recommended. Nitroprusside is excellent for use in critically ill patients because of its rapid onset and offset of action (within 1-2 min). It is excellent for use against pulmonary edema associated with severe hypertension that is unresponsive to other agents.
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Radiograph shows acute pulmonary edema in a patient who was admitted with acute anterior myocardial infarction. Findings are vascular redistribution, indistinct hila, and alveolar infiltrates.
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Radiograph shows acute pulmonary edema in a patient known to have ischemic cardiomyopathy. Findings are Kerley B lines (1mm thick and 1cm long) in the lower lobes and Kerley A lines in the upper lobes.
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Radiograph demonstrates cardiomegaly, bilateral pleural effusions, and alveolar opacities in a patient with pulmonary edema.
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Radiograph shows interstitial pulmonary edema, cardiomegaly, and left pleural effusion presenting at an earlier stage of pulmonary edema.
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Lateral chest radiograph shows prominent interstitial edema and pleural effusions.
